The human colonic epithelium exists in close proximity to trillions of bacteria. Animal models and human epidemiological studies have long implicated the enteric microbiome in the etiopathogenesis of colorectal cancer (CRC). Mechanisms by which the microbiome might initiate and/or promote colon tumor development remain obscure, with evidence supporting DNA damage by oncogenic bacterial toxins and/or induction by the microbiota of select inflammatory pathways. Limited observations, to date, have supported dysbiosis in the CRC microbial community without consistent implication of an etiologic bacterial species or genus (1).
Sporadic colorectal cancer (CRC) results from accumulated DNA mutations in colonic epithelial cells. The mechanisms causing these colonic epithelial cell mutations and propagating premalignant clones have remained unclear. One prime candidate for initiation of the biologic changes defining CRC is an altered colonic microbiota that acts early in disease pathogenesis to initiate and then, over time, to promote CRC through direct effects on colonic epithelial cell biology and/or instigation of insidious chronic mucosal inflammation. However, clear associations between microbiota composition and CRC development have not been established.